The present invention is directed toward preventing infant deaths due to prolonged periodic breathing and sudden infant death syndrome.
Periodic breathing is a normal phenomenon where an infant's breathing pattern is interrupted by recurrent apneas or absences of breathing. It has been shown in independent studies that an increase in ambient oxygen concentration correlates with a reduction in the incidence of apnea in infants. Kattwinkel, J., Neonatal/Apnea: Pathogenesis and Therapy, 90 J. Pediatric 342 (1977); Hoppen-Brouwers, T., Hodgman, J. E., Harper, R. M., et al., Polygraphic Studies of Normal Infants During the First Six Months of Life: I. V. Incidence of Apnea and Periodic Breathing, 60 Pediatrics 418 (1977). Pharmacological therapies have been used to treat prolonged periodic breathing, but the effect of these therapies remains uncertain. Neil N. Finer, M.D., Keith J. Barrington, M.D., and Barbara Hayes, R.N., Prolonged Periodic Breathing: Significance in Sleep Studies, Pediatrics, Vol. 89, No. 3, pp. 450-52 (March 1992).
Sudden infant death syndrome is defined as the sudden, unexpected death of a previously healthy infant which cannot be explained by a review of the child's medical history, a death scene investigation or a thorough postmortem examination. Sally L. Davidson Ward, M.D., Daisy B. Bautista, CPFT, and Thomas G. Keens, M.D., Hypoxic Arousal Responses in Normal Infants, Articles from the Division of Neonatology and Pediatric Pulmonology, Childrens Hospital Los Angeles, University of Southern California School of Medicine (1991). By definition, then, the cause of sudden infant death syndrome is unknown, but several factors have been identified as being significantly associated with sudden infant death syndrome including sleeping in the prone position, failure to arouse in response to changes in oxygen level (hypoxic arousal), and overheating. James S. Kemp, M.D. and Bradley T. Thach, M.D., Sudden Death in Infants Sleeping on Polystyrene-Filled Cushions, The New England Journal of Medicine (Jun. 27, 1991); AAP Task force on Infant Positioning and SIDS: Positioning and SIDS, American Academy of Pediatrics (1992); Warren G. Guntheroth, M.D. and Philip S Spiers, Ph.D., Sleeping Prone and the Risk of Sudden Infant Death Syndrome, JAMA , Vol. 267, No. 17 (May 6, 1992).
A number of pathways leading to hypoxic arousal have been postulated, such as peripheral chemoreceptors to the reticular activating system, mechanoreceptors of the chest that sense increased ventilatory effort and stimulate the reticular activating system, and a direct effect of hypoxia on the central nervous system that causes arousal. Studies with small animals and infants have also associated apnea and sudden infant death syndrome with hypoventilation or underventilation characterized by shallow tidal volume (short breaths) and increased tidal end carbon dioxide (carbon dioxide pressure in the lungs). Unfortunately, there is little data, however, which explains hypoxic arousal failure in infants. Sally L. Davidson Ward, M.D., Daisy B. Bautista, CPFT, and Thomas G. Keens, M.D., Hypoxic Arousal Responses in Normal Infants, Articles from the Division of Neonatology and Pediatric Pulmonology, Childrens Hospital Los Angeles, University of Southern California School of Medicine (1991).
Devices have been disclosed for treating infants with breathing difficulties. For example, U.S. Pat. No. 3,786,809 describes a hoodlike plastic envelope that is placed over the infant's head. A flexible hose attached to the envelope delivers a breathing gas under pressure. Such devices are cumbersome and unsafe for treating an unattended, sleeping child.
Other devices for ventilating beds, such as U.S. Pat. Nos. 2,097,751 and 4,939,804, diffuse cool air or withdraw stale air from the foot of a bed. These devices merely cool or remove odors from bed-ridden persons and do not suggest the instant method and apparatus for improving the respiratory efficiency of an infant.
Prior to the instant disclosure, no method or device has been shown to safely assist, in a non-intrusive manner, the respiratory efficiency of an infant with hypoventilation, shallow tidal volume and increased tidal end carbon dioxide in the lungs, and decrease rebreathing of carbon dioxide by the child. Moreover, no other device is designed to be safely placed close to the child's head to supply mild continuous, even, positive air pressure directed at the child's mouth, nose, larynx and trachea/oropharynx to prevent a deficiency of oxygen in the crib (hypoxia) and an excessive amount of carbon dioxide in an infant's circulating blood (hypercapnia).